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pharmacology test #5 > Pharmacology of Thyroid Hormone > Flashcards

Pharmacology of Thyroid Hormone Flashcards

1
Q

Colloid contains

A

thyroglobulin

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2
Q

Synthesis and release of thyroid hormone

A
  1. Uptake of iodide ion by the gland
  2. Oxidation of iodide ion and the iodination of tyrosyl groups
  3. Condensation of iodotyrosyl residues to iodothyronyl residues in thyroglobulin
  4. Proteolysis of thyroglobulin and release of thyroxine and triiodothyronine into blood
  5. The conversion of thyroxine to triiodothyronine in peripheral tissues
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3
Q

Iodide uptake from the circulation occurs by

A

sodium-iodide symporter located in the basolatedral plasma membrane of thyroid follicle cell

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4
Q

Sodium-iodide symporter is inhibited by

A

complex anions such as perchlorate, thiocyanate, pertechnetate

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5
Q

Iodide is extruded from the thyroid follicle cell by

A

the protein pendrin (sodium-indepedent chloride/iodide transporter) located in the apical membrane

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6
Q

Pendred’s syndrome

A

the hereditary syndrome of goiter and deafness due to a deficiency or absence of pendrin

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7
Q

Oxidation of iodide to iodine is catalyzed by

A

the thyroid peroxidase enzyme complex in the presence of hydrogen peroxide

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8
Q

Secretion of thyroid hormone

A
  1. Endocytosis of colloid
  2. Proteolysis
  3. Release of hormones
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9
Q

80% of T3 is produced by

A

metabolism of T4 in peripheral tissues by types I, II and III 5’ deiodinases

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10
Q

Type I deiodinase catalyzes

A

the formation of circulating T3 used by peripheral tissues; requires selenium to function

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11
Q

Type II deiodinase is present/catalyzes

A

present in brain, hypothalamus, pituitary, placenta and brown adipose tissues; catalyzes the formation of intracellular T3

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12
Q

Type III deiodinase inactivates

A

inactives both T4 and T3 with preference for T3; metabolizes T4 to inactive rT3; high expressed in CNS, skin, fetal brain, and liver

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13
Q

Conditions and factors that inhibit 5’ deiodinase activity

A
  1. Acute and chronic illness
  2. Caloric deprivation
  3. Malnutrition
  4. Glucocorticoids
  5. beta-adrenergic blocking drugs
  6. Oral cholecystographic agents
  7. Amiodarone/PTU
  8. Fatty acids
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14
Q

Agents that increase metabolism of T4 and T3

A
  1. Rifampin
  2. Phenobarbital
  3. Carbamazepin
  4. Phenytoin
  5. Rifabutin
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15
Q

Major carrier of thyroid hormones

A

thyroxine binding globulin

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16
Q

Transthyretin

A

Tyroxine binding pre-albumin (TBPA)

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17
Q

Factors that increase the binding of thyroxine to thyroxin-binding globulin

A

estrogens, methadone, clofibrate, 5-fluorouracil, heroin, tamoxifen, liver disease, porphyria, HIV

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18
Q

Factors that decrease the binding of thyroxine to thyroxin-binding globulin

A

glucocorticoids, androgens, L-asparaginase, salicylates, mefenamic acid, fenclofenac, antiseizure medications, furosemide, acute and chronic illness

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19
Q

Allan-Herndon-Dudley syndrome

A

mutations in the transmembrane transporters of thyroid hormones that leads to an X-linked inherited syndrome of mental retardation and myopathy with low serum T4 levels

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20
Q

Symptoms of hypothyroidism

A
  1. Sluggish (progressive weakness)
  2. Low metabolic rate in many organs
  3. Complain about feeling cold
  4. Puffy face, doughy skin
  5. Hypercholesterolemia
  6. Decreased HR, SV, CO, and pulse pressure
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21
Q

Thyroid hormone deficiency before birth may lead to

A

cretinism (dwarfism with mental retardation)

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22
Q

Endemic cretinism

A

due to extreme deficiency of iodine; goiter may or not be present; high incidence of nerve deafness

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23
Q

Sporadic cretinism

A

due to failure of thyroid gland to develop normally; due to defect in synthesis of thyroid hormone; goiter present if defect in synthesis is the cause

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24
Q

Simple goiter

A

TSH levels are very high due to deficient secretion of thyroid hormone; may be due to iodine deficiency; may also be caused by a goitrogen

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25
Q

Hashimoto’s disease

A

chronic autoimmune thyroiditis; autoantibodies produced against thyroid peroxidase and less often thyroglobuline; thyroxine levels are low; TSH ishigh

26
Q

Diffuse toxic goiter

A

thyroid enlargement with hyperthyroidism (Graves’ disease)

27
Q

Nodular goiter

A

thyroid enlargment with nodules;
non-toxic: without thyroid hormone production
toxic: with thyroid hormone production (Plummer’s disease)

28
Q

Thyroid preparations

A
  1. Levothyroxine Sodium (Synthroid, Levothyroid, L-T4)
  2. Liothyronine Sodium (Cytomel, Triostat)
  3. Liotrix (Euthyroid, Thyrolar)
29
Q

Levothyroxine sodium (Synthroid, Levothyroid, L-T4, Levoxyl, Tirosint)

A

Sodium salt of synthetic thyroxine available in tablets and for injection

30
Q

Liothyronine sodium

A

Sodium salt of triiodothyronine (T3) available in tablets or injection

31
Q

Liotrix (Euthyroid, Thyrolar)

A

Mixture of sodium salts of : Levothyroxine and Liothyronine

32
Q

When would Liothyronine sodium (T3) be administered instead of Levothyroxine sodium?

A

if faster action of replacement therapy is desired: recent hypothyroidism, overtreatment with antithyroid drugs, after treatment with radioiodine, after thyroidectomy

33
Q

What do thyroid hormones do to the heart?

A

increase cardiac contractility; important to treat patients with initial low doses of levothyroxine (synthroid) until an acceptable dose is reached

34
Q

Myxedema usually caused by

A

degeneration and atrophy of thyroid gland

35
Q

When is a goiter associated with myxedema?

A

during severe defect in thyroid hormone synthesis and during chronic thyroiditis

36
Q

Myxedema is often associated with

A

coronary artery disease

37
Q

Myxedema coma

A

end-state of untreated hypothyroidism characterized by weakness, stupor, hypothermia, hypoventilation, hypoglycemia, shock and death

38
Q

Treatment of myxdema coma

A

initial large IV dose of levothyroxine to occupy that large pools of free and unoccupied thyroid hormone binding sites

39
Q

Subclinical hypothyroidism

A

an elevated TSH level in the face of normal thyroid hormone levels

40
Q

Symptoms of hyperthyroidism (thyrotoxicosis)

A

hot, thin, nervous, SOB, flushed skin, increased appetite, muscle weakness, tremor

41
Q

Diseases with hyperthyroidism

A

Graves’ disease and Plummer’s disease

42
Q

Graves’ disease

A

autoimmune disease; lymphocytes produce a TSH receptor stimulating antibody (TSI); activates thyroid gland by binding to TSH receptors and stimulating thyroid hormone production in a manner identical to that of TSH

43
Q

Plummer’s disease

A

may be associated with nodular tumors

44
Q

Treatment of Graves’ disease

A

antithyroid drugs and radioiodine (to destroy the gland)

45
Q

Categories of major antithyroid drugs

A
  1. drugs that interfere directly with thyroid hormone synthesis
  2. Ionic inhibitors: block iodide transport
  3. Iodide itself: suppresses thyroid hormone synthesis and secretion at high concentrations
  4. Iodinated contrast media: suppresses T4 to T3 converstion
  5. Radioactive iodide: destroys gland with ionizing radiations
  6. Lithium: suppresses synthesis and release of thyroid hormones
46
Q

Drugs that interfere with thyroid hormone synthesis

A
  1. Thioamides
  2. Aniline derivatives
  3. Polyhydric phenols
47
Q

Thioamides

A

PTU, Methimazole, Carbimazole

48
Q

Aniline Derivatives

A

Sulfathiazole, Sulfadiazine

49
Q

Polyhydric phenols

A

Resorcinol

50
Q

MOA of Thioamides

A

Inhibit thyroid peroxidase enzyme: interfere with the oxidation of iodide ion to iodine, interfere with the incorporation of iodine in tyrosyl groups of thyroglobulin, interfere with coupling of iodotyrosyl groups of thyroglobulin

51
Q

Difference between PTU and methimazole

A

PTU inhibits peripheral conversion of T4 to T3; methimazole does not have peripheral effects like PTU

52
Q

Preferred antithyroid agent during pregnancy

A

PTU because it crosses the placenta to a lesser extent that methiazole and it has lesser excretion in breast milk

53
Q

Toxicity of thioamides

A

nausea, GI distress, rash, fever, agranulocytosis

54
Q

Anionic inhibitors interfere with

A

the ability of the thyroid gland to concentrate iodidie ion; rarely used in clinical practice

55
Q

Anionic inhibitors

A

Thiocyanate (SCN-)
Perchlorate (ClO-4)
Nitrate (NO-3)
Fluoborate (BF-4)

56
Q

Iodide is used to

A

prepare patients of Graves’ disease for thyroidectomy (to reduce vascularity of the gland)

57
Q

Clinical effects of iodide on thyroid gland

A

Vascularity is reduced; gland becomes firm and hard to touch; follicular cells become smaller; colloid reaccumulates in follicles; quantity of bound iodine increases

58
Q

Most important MOA of iodide

A

inhibits the release of thyroid hormone

59
Q

Caution with the clinical use of iodide

A

iodide accumulates in the thyroid gland and may render later treatments with thioamides and radioactive iodine ineffective

60
Q

Iodinated contrast media

A

ipodate, diatrizoate, iohexol

61
Q

What can happen to patients being treated for psychiatric diseases with lithium salts

A

can develop hypothyroidism with a goiter due to the inhibitory effect of lithium on organification of iodide, suppression of coupling of iodothyrosine residues and the release of thyroid hormones

pharmacology test #5 (11 decks)

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